Overview of Lower Extremity Peripheral Nerve Syndromes

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Overview of lower extremity peripheral nerve syndromes

AUTHOR: Seward B Rutkove, MD
SECTION EDITOR: Jeremy M Shefner, MD, PhD
DEPUTY EDITOR: Richard P Goddeau, Jr, DO, FAHA
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: May 2024.

This topic last updated: Mar 04, 2024.
INTRODUCTION
This topic provides an overview of lower extremity peripheral nerve syndromes. Peripheral
nerve syndromes involving the upper extremities are discussed separately. (See "Overview of
upper extremity peripheral nerve syndromes".)
ANATOMY
Nerve roots emerge from the spinal column from the L2 to S4 levels through the neural
foramina and join to form a complex entity known as the lumbosacral plexus ( figure 1).
Unlike the brachial plexus, in which the anatomy is delineated through trunks, divisions, and
cords, the lumbosacral plexus has only two main components: the lumbar plexus (made up of
nerve fibers from the L2 through L5 roots) and the sacral plexus (made up of nerve fibers from
the S1 through S4 roots).
The largest nerve that emerges from the lumbar plexus is the femoral nerve, which descends
beneath the inguinal ligament before dividing into a number of smaller branches innervating
the anterior thigh musculature and skin ( figure 2). One pure sensory branch, the saphenous
nerve, continues down the medial leg to the arch of the foot. Although the subject of some
disagreement, the iliopsoas muscle is innervated by the femoral nerve or a small nerve of its
own that travels alongside the femoral. The obturator nerve also emerges from the lumbar
plexus, descending more medially than the femoral, exiting the pelvis through the obturator
foramen where it innervates the thigh adductors and a small cutaneous area in the medial
thigh.
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A small nerve, the lateral femoral cutaneous nerve, also has its origin directly from the plexus. It
travels lateral to the femoral nerve underneath the inguinal ligament to innervate the skin of
the lateral thigh.
Contributions from the lower lumbar plexus and upper sacral plexus give rise to the sciatic
nerve. This nerve passes through the sciatic foramen and descends the posterior aspect of the
leg until it reaches the popliteal fossa, where it divides into the tibial and common fibular
(peroneal) nerves.
Branches from both the lumbar and sacral plexus also form the inferior and superior gluteal
nerves innervating the lateral and posterior hip musculature. Branches from the sacral plexus
alone converge to form the pudendal nerves, innervating the pelvic floor musculature and
perineal sensation.
PATHOGENESIS
Compression — Compression (including neurapraxia and axonotmesis) is the most common

problem that affects neuronal structures in the lower extremities. Compression can affect distal
nerve segments, as occurs in tarsal tunnel syndrome or fibular (peroneal) neuropathy at the
fibular neck but is even more common proximally where a herniated disc may compress a spinal
nerve root.
In its mildest form, compression may be intermittent due to positioning, with associated
reversible ischemia of the nerve. One common situation is numbness along the lateral shin and
dorsum of the foot after crossing the legs secondary to compression of the fibular (peroneal)
nerve as it passes across the fibular neck.
Demyelination occurs as compression grows more consistent and chronic. Symptoms are
usually persistent at this point, and pain and weakness may become more prominent. As
compression progresses further, the distal nerve segments will no longer function and
Wallerian degeneration may occur. In most severe cases, the entire distal segment of the nerve
can degenerate, similar to what would be seen in a nerve transection. (See 'Transection' below.)
From a physiologic standpoint, the patient will remain asymptomatic as long as all nerve
impulses are transmitted through a region of compression. As ischemia or demyelination
occurs, nerve conduction will first be slowed, and then eventually blocked completely. Slowing
of nerve conduction has no physiologic correlate; only the complete conduction block of
neuronal impulses produces functional sensory loss or weakness. Conduction block of more
and more nerve fibers occurs as compression worsens. Eventually almost no impulses make it
through the compressed area, while distal neuronal degeneration simultaneously begins to
take place.
Transection — Acute nerve transection (also called neurotmesis) is much less common than
chronic nerve compression. It can occur with leg trauma (eg, knife wounds) as the distal nerve is
completely separated from the proximal portion. Unlike even severe cases of nerve
compression, the basement membrane of each individual nerve cell no longer remains intact
following transection; regrowth of the nerve is impossible without intervention.
Nerve ischemia/infarct — Nerve infarction generally only occurs in relation to vasculitis and
atherosclerotic disease, although it is also thought to play a role in diabetic amyotrophy (see
'Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy' below). Nerve
infarction in patients with vasculitis causes an axonal injury pattern, typically at well-defined
areas of the nerve. The most common symptomatic location for a nerve infarct in the lower
extremity is the sciatic nerve in the midthigh; more distal infarctions in the fibular (peroneal)
and tibial nerves also occasionally occur.
Unlike the case of compressive neuropathy, conduction velocity slowing does not occur. The
entire distal segment of the nerve degenerates within a few days of focal nerve infarction.
However, since the basement membrane remains intact, regrowth of the nerve may occur with
control of the underlying disease.
Radiation-induced injury — Radiation exposure, generally in the context of radiotherapy for

neoplastic disease, can result in nerve damage that may not appear clinically for years after the
procedure. Although more common in patients who have undergone axillary radiation therapy
for breast cancer, it can also occur in the lower extremities after receiving pelvic irradiation (eg,
for cervical cancer). Progressive weakness and sensory loss with marked proprioceptive
dysfunction may occur.
Inflammation — Inflammatory processes of the nerve or roots also can cause significant
problems affecting the legs.
● Infectious disorders such as herpes simplex, Epstein-Barr virus, and most commonly
herpes zoster virus can produce syndromes of sensory loss and motor dysfunction.
● An idiopathic inflammatory response is responsible for the syndrome of lumbosacral

plexitis.
● An inflammatory response associated with diabetes mellitus occasionally occurs, likely

playing a role in diabetic radiculopathy and diabetic amyotrophy.

● Inflammation restricted to the dorsal root ganglion may occur rarely as a paraneoplastic
process or associated with Sjögren's disease.
Degeneration — Distal degeneration of neurons is the hallmark of most axonal

polyneuropathies. Gradual deterioration of neurons occurs in a distal to proximal fashion, with
the longest nerves affected first. The reason proposed for this phenomenon is that the most
distal segments of nerve are the most vulnerable to metabolic and toxic factors.
Proximal degeneration of neurons also may occur in certain disorders, although this is much
less common. Most concerning is a focal form of motor neuron cell loss associated with
progressive weakness of an entire extremity over a period of months; this may represent a focal
form of motor neuron disease.
EPIDEMIOLOGY
Data on the epidemiology of lower extremity peripheral nerve syndromes are relatively limited.
The most common nerve problem affecting the lower extremities is probably lumbosacral
radiculopathy ( table 1). Low back pain is an extremely common complaint (significantly
affecting between 40 to 80 percent of people at some time), although clinically apparent
lumbosacral radiculopathy is less common, perhaps affecting 4 to 6 percent of the population at
some point in their lives [1]. The next most common problem, excluding polyneuropathy, is
likely to be compression of the fibular (peroneal) nerve at the fibular neck ( table 2). In our
electromyography (EMG) laboratory, this diagnosis accounted for approximately 2 percent of all
referrals over a one-year period. Postpartum compression neuropathies, most frequently
involving femoral or lateral femoral cutaneous nerves, have been reported in 1 to 58 per 10,000
deliveries [2]. The true incidence is not known since most series relied upon patient surveys or
medical record discharge coding. There are no published data that identify the frequency of
plexopathy or other entrapment neuropathies affecting the lower extremities.
CLINICAL PRESENTATION
The signs and symptoms suggestive of a peripheral nerve problem are discussed in detail
separately. (See "Evaluation of peripheral nerve and muscle disease".)
Specific syndromes are summarized in the tables ( table 1 and table 2) and discussed in
detail below.

Very mild focal abnormalities of the lower extremity nerves may be identified when performing
electrophysiologic testing for other purposes (eg, to look for polyneuropathy). As an example,
fibular (peroneal) motor conduction velocity slowing across the fibular neck segment may
suggest extremely mild compression of the nerve. Lumbosacral radiculopathy is probably the
most common asymptomatic problem identified, especially in older individuals.
DIAGNOSTIC TESTING
Electrodiagnostic studies — Electromyography (EMG) and nerve conduction studies (NCS)

remain the most effective means of identifying and classifying peripheral nerve disorders
affecting the lower extremity. (See "Evaluation of peripheral nerve and muscle disease".)
Focal entrapments of the fibular (peroneal) nerve are generally straightforward to determine
using EMG/NCS. The electromyographer looks for evidence of demyelination (conduction
velocity slowing and conduction block) across likely affected segments of nerve, such as the
fibular (peroneal) nerve at the fibular neck. EMG tends to be most important for the diagnosis of
radiculopathy and plays a more confirmatory role in other disorders. It will give some insight
into lesion severity as well.
In plexopathies, abnormalities are usually found in several nerves emanating from one region
of the plexus. Studying conduction across the plexus is generally not performed for technical
reasons; thus, the usual findings of demyelination cannot be sought. Instead, testing is
confined to distal segments and a search for axon loss is pursued. As an example, in a patient
with a diffuse lumbosacral plexopathy, reductions in the amplitude of the sural, superficial
fibular (peroneal), and saphenous sensory responses are typical. Needle examination may
disclose fibrillation potentials and positive sharp waves in multiple lower extremity muscles not
confined to one limb or myotome.
In radiculopathy, sensory responses are spared since the lesion is proximal to the dorsal root
ganglion. Motor studies are usually also normal, although L5 radiculopathy can produce a
reduction in amplitude of the extensor digitorum brevis motor response when stimulating the
fibular (peroneal) nerve. Usually abnormalities are identified only on needle examination of the
muscles derived from the affected roots.
Imaging — Imaging is the best first study to obtain in patients with a suspected structural
cause to symptoms. As an example, magnetic resonance imaging (MRI) of the lumbosacral
spine is reasonable in a patient with a radiculopathy who has radiating back pain, sensory loss
over the dorsum of the foot, and weakness in L5 muscles. In addition, one-time imaging is

probably warranted in patients with idiopathic plexopathies to exclude the possibility of a mass
lesion in the region, especially in those with worsening symptoms or a history of neoplastic
disease.
However, in most situations a patient's complaints are more nondescript. Pain may be nonfocal,
weakness minimally present, and no fixed sensory loss identified. In these situations EMG/NCS
is probably the first test to pursue and, depending upon the results, imaging of the appropriate
area can be performed secondarily. For example, MRI of nerves may be performed after
EMG/NCS has suggested a specific location for the problem, such as a midthigh sciatic
neuropathy. MR neurography can provide information on deeper neuronal structures that may
be hard to access via ultrasound; it should also be considered a useful alternative if other
diagnostic methods are proving insufficient information [3].
● Magnetic resonance imaging – MRI is the mainstay of most peripheral nerve imaging. In
lumbosacral spine disease, specifics of disc herniation, degeneration, and degree of
compression of a specific nerve root have made this tool invaluable, especially when
considering a surgical option. In one study, the degree of herniation on MRI was
correlated with the patient's symptoms and improvement [4]. On the other hand, another
report that compared MRI and EMG in the diagnosis of radiculopathy found that the two
procedures were in agreement only 60 percent of the time, with a significant abnormality
being identified on one test and not the other in 40 percent of cases [5].
● Ultrasound – Ultrasound is also very useful for the study of compressive, inflammatory,
and traumatic neuropathies, and can identify neoplastic changes in nerves as well. With
high-resolution ultrasound transducers, nerves in the lower extremity can be followed
from the gluteal region to the foot, but given the large diameter of the legs and the
thickness of the feet and sole, it is more difficult to resolve proximal nerves and terminal
branches. High-resolution ultrasound is particularly informative with respect to nerve
compression syndromes; focal nerve enlargement (increased cross-sectional area) and loss
of echogenicity are useful indicators of pathology. As an example, a case-control study of
40 subjects with common fibular (peroneal) neuropathy found that the diagnostic accuracy
of ultrasound was similar to that of MRI [6]. (See "Diagnostic ultrasound in neuromuscular
disease", section on 'Findings in normal nerves' and "Diagnostic ultrasound in
neuromuscular disease", section on 'Findings in neuropathy'.)
Computed tomography (CT) has some utility for patients with pacemakers or those who cannot
use an MRI for other reasons. CT combined with myelography gives useful information
regarding nerve roots in patients with lumbosacral disc disease but is rarely performed today.
CT can also give better information about bony elements than MRI does.
Serologic testing — Serologic testing is usually of limited value in patients presenting with
focal symptoms affecting a limb. However, some tests are worth considering:
● Fasting glucose and glycohemoglobin in patients with possible diabetic amyotrophy,

idiopathic radiculopathy, polyneuropathy
● Lyme titers in patients with polyradiculopathy, especially in endemic areas
● Hereditary neuropathy with predisposition to pressure palsy gene test in patients with
multiple mononeuropathies (usually affecting at least two to three extremities)
In patients with mononeuropathy multiplex, many other laboratory studies are warranted in an
attempt to identify the underlying disorder.
Lumbar puncture — Lumbar puncture is warranted in patients with unusual presentations of

radiculopathy or where distinguishing between a radiculopathy and lumbosacral plexopathy is
not straightforward. The cerebrospinal fluid (CSF) should be examined for evidence of
inflammation (including elevated CSF protein and mononuclear cells) and serologic testing for
Lyme disease, syphilis, and cytomegalovirus (CMV).
FIBULAR (PERONEAL) NERVE
Compression at the fibular neck — The most frequent site of injury to the common fibular
(peroneal) nerve is just below the knee as the nerve wraps around the lateral aspect of the
fibula, immediately before dividing into its deep and superficial branches. Compression at this
site is frequently produced by external pressure on the nerve due to prolonged lying, such as
during surgery, palmar pressure to the fibular neck during childbirth, or prolonged
hospitalization. Crossing the legs, protracted squatting, and leg casts also can cause
compression at this site.
● Clinical features – The typical clinical presentation of common fibular (peroneal)

neuropathy at the fibular neck is acute foot drop (difficulty dorsiflexing the foot against
resistance or gravity). Patients describe the foot as limp; there is a tendency to trip over it
unless they compensate by flexing the hip higher when walking, producing what is called a
"steppage" gait. Patients may also complain of paresthesias and/or sensory loss over the
dorsum of the foot and lateral shin (superficial fibular (peroneal) nerve territory) [7]. In one
study, 79 percent of 103 patients with common fibular (peroneal) neuropathy complained
of sensory loss; pain was relatively infrequent, affecting only 17 percent [8].

● Evaluation – Examination typically reveals weakness in foot dorsiflexion and foot eversion
(deep and superficial fibular (peroneal) nerve-innervated, respectively), with normal
inversion and plantar flexion (tibial nerve). Sensory disturbance is confined to the dorsum
of the foot, including the web space between digits 1 and 2 and the lateral shin. Reflexes
are normal.
Electromyography (EMG) and nerve conduction studies (NCS) are very useful for
identifying fibular (peroneal) neuropathy at the fibular neck; conduction block on fibular
(peroneal) motor studies may be identified at the site, even in the acute setting. Reduction
in distal motor and sensory response amplitudes can occur in severe cases, suggesting
axonal injury. Needle examination discloses abnormalities in the deep and superficial
fibular (peroneal) nerve innervated muscles.
● Treatment – In contrast to upper extremity neuropathies, treating compression

neuropathies of the lower extremity is often not possible or of limited benefit. In patients
with a fibular (peroneal) neuropathy at the fibular neck, for example, no specific treatment
is available other than removing pressure on the nerve (such as extra cushioning while
sleeping and avoidance of crossing the legs during the day). An ankle-foot orthosis splint,
to keep the foot dorsiflexed, should be used until active movement has recovered. Physical
therapy progressing from passive range of movement to passive-assistive, active, and
active-resistance exercise under supervision with a physical therapist may also be helpful.
Walking is particularly important therapy.
Operative decompression can be considered for patients who do not recover on their own,
although true entrapment of the fibular (peroneal) nerve is uncommon. One investigator,
for example, explored 26 common fibular (peroneal) nerves in 23 patients; evidence for
entrapment was found in only one of the eight with no other apparent cause for the
neuropathy [9]. Entrapment should be suspected when symptoms and signs progress and
no other cause is identified. In that circumstance, surgical decompression can be
successful [10].
● Prognosis – Prognosis depends upon the degree of dysfunction. In one study of 13

patients with idiopathic common fibular (peroneal) palsy, those presenting with complete
lesions (no preserved function in foot dorsiflexion and foot eversion) made no significant
recovery, while patients with even mildly preserved strength recovered fully [11].
Compression at the ankle — The deep fibular (peroneal) nerve is rarely injured in the region of
the ankle. Usually injury is due to a tight-fitting rim or strap from a shoe. Patients generally
complain of pain in the region with minimal weakness and sensory disturbance involving only

the web space between digits 1 and 2. Directed physical examination reveals minimal
abnormalities. NCS may demonstrate a prolonged distal motor latency; on needle EMG,
abnormalities can be identified in extensor digitorum brevis.
Popliteal lesions — Injury to the common fibular (peroneal) nerve occasionally occurs in the
popliteal fossa, immediately after the division of the sciatic nerve into tibial and common fibular
(peroneal) nerves. Baker's cysts are the most common cause in this region. Nerve infarctions
due to mononeuropathy multiplex also occur in the area of the knee and, at least acutely, may
be difficult to distinguish from a compressive neuropathy at the fibular neck, although pain is
prominent in vasculitic lesions and is minimal in compressive ones.
TIBIAL NERVE
Tarsal tunnel syndrome — Tarsal tunnel syndrome refers to tibial nerve compression in the
region of the ankles as the nerve passes under the transverse tarsal ligament ( figure 3).
Beneath this retinaculum (or laciniate ligament) lies a tunnel containing the tendons of the
flexor digitorum longus and flexor hallucis longus muscles, the vascular bundle, the tibial nerve,
and the medial and lateral plantar nerves. The most common cause of tarsal tunnel syndrome is
a fracture or dislocation involving the talus, calcaneus, or medial malleolus. In these cases, scar
tissue, bone or cartilage fragments, or bony spurs may be found compressing the nerve.
Etiologies other than injury include rheumatoid arthritis, other causes of inflammation, and
tumors.
● Clinical features – Patients with tarsal tunnel syndrome typically present with aching,
burning, numbness, and tingling involving the sole of the foot, the distal foot, the toes,
and occasionally the heel. The pain may radiate up to the calf or higher [12]. The
discomfort is often most irritating at night, may be worse after standing, and sometimes
leads to the desire to remove the shoes, even while driving.
● Evaluation – Examination may disclose a prominent Tinel sign over the nerve posterior to
the medial malleolus with sensory loss over the plantar surface of the foot, not extending
onto the dorsal foot. Atrophy of intrinsic foot musculature will be present only if the nerve
injury is severe.
Although it is a common consideration in patients presenting with foot and ankle pain,
making a definite diagnosis of this disorder is difficult. Electrodiagnostic testing may reveal
prolonged tibial motor distal latencies and slowing of conduction velocities across the
flexor retinaculum when recording from the medial and lateral plantar nerve territories.

Comparison studies with the unaffected extremity may be helpful in this regard.
Electromyography (EMG) evaluation is of limited utility since the intrinsic foot muscles
normally have mild degrees of denervation and chronic reinnervation. Again, comparison
with the appearance of foot musculature on the contralateral limb is usually necessary.
In general, true tarsal tunnel syndrome is most commonly diagnosed in patients with a
clear history of antecedent foot trauma. Without such a history, "idiopathic" tarsal tunnel
syndrome, unlike carpal tunnel syndrome, is quite rare.
● Treatment — Patients with symptoms of tarsal tunnel syndrome and no history of trauma
should be given a trial of conservative therapy, including nonsteroidal antiinflammatory
drugs (NSAIDs), shoe modification, and in some cases orthotics. If the patient does not
respond, corticosteroid injection may provide relief and can be useful diagnostically.
Decompression of the tibial nerve at the ankle is effective in some patients who truly have
a documented entrapment and have failed conservative therapy. In one retrospective
study, 47 patients over a 10-year period underwent surgical decompression of the tibial
nerve at the ankle after an average 16 months of conservative therapy [13]. The majority
(81 percent) had confirmatory nerve conduction abnormalities with suggestive clinical
findings (including a Tinel sign at the ankle). In general, patients noted an improvement in
symptoms, with 72 percent stating that they were satisfied with the surgical outcome.
However, the perioperative complication rate was very high at 30 percent.
Other surgical studies have noted more mixed results. The most favorable outcomes
appear to occur with a short history of illness, the presence of a ganglion, no history of
sprains, and light work demands [14]. In a small randomized controlled trial of patients
with painful diabetic polyneuropathy, foot pain, and presumed tarsal tunnel syndrome,
decompression of the tarsal tunnel resulted in no significant change in the cross-sectional
area of the tibial nerve based upon ultrasound data [15].
Other tibial nerve injuries — The tibial nerve is rarely affected more proximally due to its deep
location within the lower leg. Like the fibular (peroneal) nerve, however, occasional compressive
symptoms can occur in the popliteal fossa, such as from a Baker's cyst.
Isolated medial and lateral plantar neuropathies may also occur within the foot itself. These
often are due to trauma, fibrosis, or possibly entrapment.
SCIATIC NERVE
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Sciatic neuropathy occurs due to a variety of causes.
● In one study of 73 patients who fulfilled strict electrophysiologic criteria for sciatic
neuropathy, hip surgery was the cause in 22 percent, acute external compression in 14
percent, infarction in 10 percent, gunshot wound in 10 percent, hip fracture/dislocation in
10 percent, femur fracture in 4 percent, possible contusion in 4 percent, and unclear
etiology in 16 percent [16].
● In another report of sciatic nerve lesions in 53 children, the etiologies included trauma in
25 percent, iatrogenic causes (orthopedic and other surgeries) in 25 percent, tumor in 13
percent, prolonged external compression and immobilization in 11 percent, vascular in 9
percent, idiopathic and progressive in 8 percent, unknown (presumed viral) in 6 percent,
and infantile and nonprogressive in 4 percent [17].
● Other uncommon causes of sciatic neuropathy include childbirth, vascular malformations,

injury to the biceps femoris muscles, and endometriosis [18-24].
Compression/trauma in the sciatic notch/gluteal region — The most common cause for
compression or injury to the sciatic nerve in this region is trauma, including hip dislocation,
fracture, or replacement. Other etiologies include wayward buttock injections, compression by
external sources such as prolonged bed rest (eg, coma), and any deep-seated mass in the pelvis,
including hematomas.
The piriformis syndrome is a controversial condition that may be an occasional contributor to

sciatic nerve injury [25,26]. In this disorder, compression of the sciatic nerve occurs in the region
of the sciatic notch as the nerve comes in close contact with a hypertrophied piriformis muscle.
However, there is no consensus about diagnostic criteria, and the diagnosis remains one of
exclusion.
Sciatic nerve lesions also have been reported as an unusual complication of cardiac surgery. In
one study, six cases of postcardiac surgery sciatic neuropathy were identified over a 15-year
period [12]. An intraaortic balloon pump was used on the ipsilateral side in four of these
instances. The majority of affected patients also had symptomatic peripheral vascular disease.
● Clinical features – In addition to pain, patients with significant injury to the sciatic nerve
in this region also complain of weakness affecting most of the lower leg musculature,
including the hamstrings. Hip flexion, extension, abduction and adduction, and knee
extension are normal. Sensory loss involves the entire fibular (peroneal), tibial, and sural
territories. In the lower leg, however, the medial calf and arch of the foot may be spared
secondary to innervation by the preserved saphenous nerve (a branch of the femoral

nerve). Sensation is also spared above the knee both anteriorly and posteriorly. The knee
jerk is normal, but the ankle jerk is unobtainable.
● Evaluation – Compression of the sciatic nerve may not produce significant abnormalities
on electromyography (EMG) unless it is relatively severe. Reduced fibular (peroneal) and
sural sensory responses and a normal saphenous sensory response are identified in more
severe cases. Tibial and fibular (peroneal) motor response amplitudes also are reduced. A
denervation/reinnervation pattern in muscles supplied by the nerve, including the
hamstrings, is typical.
● Management – Treatment varies by underlying cause. Acute symptoms may improve with
treatment of underlying structural cause such as femur fracture, tumor, or hematoma.
Supportive therapy consists of physical therapy. The prognosis of sciatic neuropathy is
generally favorable. In one study, patients had a 75 percent overall likelihood of good
recovery without treatment over a three-year period [16]. Absence of paralysis in foot
plantar flexion and dorsiflexion at initial evaluation was a favorable prognostic sign.
Lesions in the midthigh — Sciatic nerve lesions less commonly occur in the midthigh.
Etiologies include compression due to a femur fracture or mass, or ischemic nerve infarction.
Symptoms and signs may be very similar to those caused by sciatic nerve injury in the gluteal
region except that some sparing of hamstring function is likely. Interestingly, the predominant
abnormalities in sciatic nerve function often affect the fibular (peroneal) more than the tibial
division, even though the entire sciatic nerve is affected. This is often true electrophysiologically
as well as clinically.
FEMORAL NERVE
Compression of the femoral nerve is relatively uncommon due to its position within the pelvis
and anterior thigh. Nevertheless, hip or pelvic fractures or masses within the iliacus (such as
hematoma) can sometimes result in a femoral neuropathy. The true incidence of iatrogenic
femoral nerve injury is unknown, but the syndrome is a recognized complication of childbirth
and procedures such as hip replacement, abdominal and pelvic surgery or laparoscopy, inguinal
lymph node biopsy, femoral nerve block, and femoral artery puncture [2,27,28]. In addition to
compression, other potential mechanisms of iatrogenic femoral nerve injury include
transection, diathermy, toxic injury, and ischemia [27,28]. In a review of 159 patients with
femoral neuropathy, the most common causes were compression (40 percent), perioperative
injury (35 percent), and inflammation (6 percent) [29].

Factors that appear to predispose pregnant patients to femoral neuropathy postpartum include
fetal macrosomia or malpresentation, sensory blockade (can impair recognition of discomfort),
prolonged lithotomy position, or prolonged second stage. However, many of these factors are
interdependent (eg, prolonged lithotomy position and prolonged second stage) [30].
Patients with diabetes mellitus occasionally develop spontaneous femoral neuropathies.

However, it is debated whether this simply represents a more limited form of diabetic
amyotrophy (see 'Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy'
below). The mechanism of this is presumably nerve infarction.
● Clinical features and evaluation – Patients with significant femoral neuropathies develop
knee extension weakness involving the quadriceps muscle group with sparing of
adduction as well as hip flexion weakness [29]. One argued point is whether or not the
iliopsoas is innervated by the femoral nerve or a direct branch of the plexus; regardless of
the strict answer, it is clear that some patients with what appear to be isolated femoral
neuropathies also have prominent iliopsoas weakness. In addition to muscle weakness,
sensory loss over the anterior thigh and most of the medial thigh is typical. The sensory
loss extends down the medial shin to the region of the arch of the foot due to saphenous
nerve dysfunction. The knee jerk generally decreases or becomes unobtainable.
Occasionally the infrapatellar branch of the saphenous nerve is damaged due to mild
trauma or knee operations. This produces the syndrome of gonyalgia paresthetica, which
includes sensory loss in a several centimeter diameter patch below the knee with
intermittent lancinating pains [31].
Needle electromyography (EMG) may be helpful in demonstrating isolated involvement of

muscles innervated by the femoral nerve without involvement of obturator innervated
muscles or paraspinals. A reduced or absent saphenous sensory response will also help
confirm the presence of a femoral neuropathy.
● Management – The management of femoral nerve injury is mainly supportive and

includes physical therapy, but depends in part upon the mechanism and severity of injury
[27-29]. A compressive hematoma may require drainage with correction of any underlying
coagulopathy. Analgesia is indicated for patients with significant pain. Surgical exploration
and nerve repair or grafting may be needed for patients with suspicion of traumatic direct
nerve injury, such as transection or ligation.
● Prognosis – The prognosis of incomplete femoral nerve injury is generally good [27,28].
The degree of axon loss as determined by electrodiagnostic studies is an important
prognostic indicator. In one series of 31 patients with unilateral femoral neuropathy,
excellent, satisfactory, and poor outcomes were observed in 31, 34, and 31 percent,
respectively [32]. The only factor associated with prognosis was the estimate of axonal
loss.
LATERAL FEMORAL CUTANEOUS NERVE
The lateral femoral cutaneous nerve is a small sensory nerve that is a direct branch of the
lumbar plexus. Entrapment of the nerve as it traverses below the inguinal ligament produces
the common syndrome of meralgia paresthetica. Some people are especially predisposed to
developing meralgia paresthetica, including those with obesity, diabetes mellitus, and advanced
age. Pregnant and postpartum patients are also at increased risk. In others, no obvious cause is
identified. (See "Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)", section
on 'Causes and risk factors'.)
● Clinical features – Patients generally complain of paresthesias and pain that radiates
down the lateral aspect of the thigh toward the knee. The pain can be quite significant. In
more advanced cases, fixed sensory loss on the lateral thigh occurs. (See "Meralgia
paresthetica (lateral femoral cutaneous nerve entrapment)", section on 'Clinical features'.)
● Evaluation – The diagnosis of meralgia paresthetica is based primarily upon the unique
description of pain and characteristic locations, sensory abnormalities on examination,
and absence of neurologic abnormalities of the lower leg. Electrodiagnostic studies have a
limited role in the evaluation of this disorder. Studies may be relatively normal in mild
cases. A reduced response amplitude is generally evidence for a lesion severe enough to
produce axon loss. Needle electromyography (EMG) is performed to help exclude
radiculopathy or plexopathy. (See "Meralgia paresthetica (lateral femoral cutaneous nerve
entrapment)", section on 'Diagnosis'.)
● Management – Meralgia paresthetica is a self-limited, benign disease in most patients.

More than 90 percent of patients respond to conservative measures such as weight loss
and avoiding external pressure over the inguinal ligament (eg, due to supporting heavy
materials on the thigh). However, recurrent symptoms are common. Anticonvulsants such
as carbamazepine, phenytoin, or gabapentin may be helpful in reducing neuropathic pain
for patients with persistent symptoms despite conservative measures. A local nerve block
can also be considered. Rarely, surgical nerve decompression or sectioning is used. (See
"Meralgia paresthetica (lateral femoral cutaneous nerve entrapment)", section on
'Treatment'.)

OBTURATOR NERVE
Mononeuropathies of the obturator nerve are uncommon. They present with pain, weakness in
leg adduction, and sensory loss over a small area in the medial thigh. There is no compelling
evidence of a true obturator entrapment neuropathy caused by a narrow obturator foramen
[33]. However, obturator neuropathy does occur secondary to pelvic trauma or surgery. In
addition, one study suggested that isolated obturator neuropathy can be the sole manifestation
of pelvic cancer, most commonly transitional cell carcinoma of the bladder [34]. (See "Nerve
injury associated with pelvic surgery", section on 'Obturator nerve'.)
LUMBOSACRAL PLEXOPATHY
Lumbosacral plexopathy is reviewed briefly here, and discussed in greater detail elsewhere. (See
"Lumbosacral plexus syndromes".)
Lumbosacral plexopathy usually presents with diffuse weakness of the affected lower extremity,
although a patchy distribution of weakness may occur. Weakness can involve the femoral and
sciatic territories depending upon whether the lumbar and sacral plexi are both involved.
Lumbar plexus lesions tend to cause weakness of hip flexion and adduction and/or knee
extension. Lumbosacral trunk and upper sacral plexus lesions result in foot drop or flail foot,
depending on the extent of involvement, and weakness of knee flexion or hip abduction.
The causes of lumbosacral plexopathy are numerous and diverse ( table 3). Important
considerations include the following:
● Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy (see "Diabetic

amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy")
● Neoplastic invasion (see "Lumbosacral plexus syndromes", section on 'Neoplastic invasion')
● Radiation therapy (see "Lumbosacral plexus syndromes", section on 'Radiation

plexopathy')
● Trauma (see "Lumbosacral plexus syndromes", section on 'Trauma')
● Pregnancy (see "Lumbosacral plexus syndromes", section on 'Peripartum plexopathy')
● Surgery (see "Lumbosacral plexus syndromes", section on 'Postoperative plexopathy')

● Vascular conditions, particularly retroperitoneal hematoma (see "Lumbosacral plexus

syndromes", section on 'Vascular causes' and "Lumbosacral plexus syndromes", section on
'Retroperitoneal hematoma')
● Parainfectious, inflammatory, and infiltrative disorders (see "Lumbosacral plexus

syndromes", section on 'Infectious, inflammatory, and infiltrative causes')
Information from the clinical setting and the physical and neurologic examinations should be
used to direct the diagnostic evaluation of lumbosacral plexopathy, which may include
laboratory studies, neuroimaging, and electrodiagnostic studies. Magnetic resonance imaging
(MRI) is the imaging method of choice for plexus evaluation given its versatility and improved
anatomic detail. However, computed tomography (CT) may be more readily available than MRI
and remains the optimal choice for those with contraindications to MRI. Electrodiagnostic
studies can help differentiate a plexopathy from lumbosacral radicular and individual nerve
syndromes, and may also provide clues to the intraplexus location and possible etiology. (See
"Lumbosacral plexus syndromes", section on 'Diagnosis'.)
DIABETIC AMYOTROPHY AND IDIOPATHIC LUMBOSACRAL RADICULOPLEXUS

NEUROPATHY
Diabetic amyotrophy and the similar condition known as idiopathic lumbosacral radiculoplexus
neuropathy are discussed briefly here and reviewed in detail separately. (See "Diabetic
amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy".)
Diabetic amyotrophy is not a pure lumbosacral plexopathy because it also affects the
lumbosacral nerve roots and peripheral nerves. The most likely cause of diabetic amyotrophy
and the clinically similar condition of idiopathic lumbosacral radiculoplexus neuropathy is
ischemic injury from a nonsystemic microvasculitis.
Diabetic amyotrophy typically occurs in patients with type 2 diabetes mellitus. The traditional
features include the asymmetric, focal onset of pain followed by weakness involving the
proximal leg, with associated autonomic failure and weight loss. Progression occurs over
months and is followed by partial recovery in most patients. However, onset in the distal leg is
not uncommon. Furthermore, the condition becomes more widespread and symmetric with
time. In nearly all cases, the symptoms and signs progress to affect the contralateral limb and
the distal legs. Thoracic and upper limb involvement has also been observed as part of the
syndrome of diabetic amyotrophy in a minority of patients. Some have symptoms and signs
suggesting a thoracic radiculopathy, a brachial plexopathy, or mononeuropathies of the ulnar

and median nerves. Most upper limb symptoms occur in association with lumbosacral plexus
involvement. (See "Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus
neuropathy", section on 'Clinical features'.)
Idiopathic lumbosacral radiculoplexus neuropathy is similar to diabetic amyotrophy with

respect to its clinical features, prognosis, and management. (See "Diabetic amyotrophy and
idiopathic lumbosacral radiculoplexus neuropathy".)
The diagnosis of diabetic amyotrophy is mainly based upon the presence of suggestive clinical
features in a patient with known or newly diagnosed diabetes mellitus. Appropriate laboratory
investigations, particularly electrodiagnostic studies, and neuroimaging in select patients, are
useful to exclude other peripheral and central nervous system etiologies as a cause of the
neurologic symptoms and signs. In patients who do not have diabetes, idiopathic lumbosacral
radiculoplexus neuropathy is the primary consideration in the differential diagnosis. (See
"Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy", section on
'Diagnostic evaluation'.)
While clinical improvement is the rule with diabetic amyotrophy and idiopathic lumbosacral
radiculoplexus neuropathy, most patients do not recover completely. There are no proven
effective treatments for these conditions. (See "Diabetic amyotrophy and idiopathic lumbosacral
radiculoplexus neuropathy", section on 'Treatment' and "Diabetic amyotrophy and idiopathic
lumbosacral radiculoplexus neuropathy", section on 'Prognosis'.)
LUMBOSACRAL RADICULOPATHY
Lumbosacral radiculopathy is a condition in which a disease process affects the function of one
or more lumbosacral nerve roots. It is reviewed briefly in the following sections, and discussed
in greater detail elsewhere. (See "Acute lumbosacral radiculopathy: Etiology, clinical features,
and diagnosis".)
Structural spine disease — Lumbosacral radiculopathy can have variable presentations. In the
young individual with an acute herniated disc, severe radiating pain, sensory loss, and weakness
in muscles of the myotome of the affected nerve root can occur ( figure 4). A specific injury or
inciting event may be recalled. Acute disc herniation is uncommon in older individuals;
spondylosis secondary to disc degeneration, calcification, and osteophytes is more typical.
● Clinical features and evaluation – Generally these patients present with sensory loss,
weakness, and pain that can be quite severe, although in some the pain is relatively
limited. Unlike the acute herniated disc of a young person in whom only one root is
affected, involvement of multiple myotomes is usually present in older people. Regardless

of age, coughing, sneezing, or leg straightening can exacerbate symptoms. The symptoms
and signs of lumbosacral radiculopathy vary according to level:
• L2-L4 radiculopathy – Localizing a midlumbar radiculopathy to a specific nerve root

can be difficult clinically and electrodiagnostically. Thus, these radiculopathies are
generally considered as a group. Acute back pain is the most common presenting
complaint, often radiating around the anterior aspect of the leg down into the knee
and possibly down to the foot. On examination, strength can be reduced in hip flexion,
knee extension, and leg adduction. Sensation may be reduced over the anterior thigh
down the medial aspect of the shin. A reduced knee jerk is commonly present in more
severe lesions.
• L5 radiculopathy – L5 radiculopathy is by far the most common radiculopathy

affecting the lumbosacral spine. It often presents with back pain that radiates down the
lateral aspect of the leg into the foot. On examination, strength can be reduced in foot
dorsiflexion, toe extension, foot inversion, and foot eversion. Mild weakness in leg
abduction may also be evident in severe cases due to involvement of gluteus minimus
and medius. Atrophy may be subtle; it is most readily observed in extensor digitorum
brevis. Sensory loss is confined to the lateral shin and dorsum of the foot. Reflexes are
generally normal.
• S1 radiculopathy – In S1 radiculopathy, pain radiates down the posterior aspect of the

leg into the foot from the back. On examination, strength may be reduced in leg
extension (gluteus maximus), foot inversion, plantar flexion, and toe flexion. Sensation
is generally reduced on the posterior aspect of the leg and the lateral foot. Ankle jerk
loss is typical.
• S2-S4 radiculopathy – Structural radiculopathies at these lower levels are distinctly less
common than other lumbosacral radiculopathies, unless a large central disc is
compressing the nerve roots intrathecally at a higher level (eg, L5). Patients can present
with sacral or buttock pain that radiates down the posterior aspect of the leg or into the
perineum. Weakness may be minimal, with urinary and fecal incontinence as well as
sexual dysfunction.
● Management – The management of structural spine disease depends upon the severity of
the lesion. Acute lumbosacral radiculopathy caused by disc herniation or foraminal
stenosis is often extremely painful, but the likelihood of spontaneous improvement is high.
Symptoms limited to pain and/or sensory loss should first be managed conservatively. The

treatment of acute lumbosacral radiculopathy is discussed in detail separately. (See "Acute

lumbosacral radiculopathy: Treatment and prognosis".)
For patients with persistent disabling lumbar radicular symptoms (eg, recalcitrant pain, leg
weakness, or impairment of bowel/bladder function) who desire surgery and are good
candidates, open discectomy or microdiscectomy are both reasonable options. (See
"Subacute and chronic low back pain: Surgical treatment".)
More general issues related to the management of low back pain, particularly nonspecific and
musculoskeletal low back pain, are reviewed elsewhere. (See "Treatment of acute low back pain"
and "Subacute and chronic low back pain: Nonsurgical interventional treatment" and
"Management of subacute and chronic low back pain" and "Subacute and chronic low back pain:
Surgical treatment".)
Nonstructural disease — Nonstructural causes are occasionally responsible for symptoms of

lumbosacral radiculopathy, although this is far less common than structural spine disease.
Neoplastic or infectious etiologies of radiculopathy require prompt mechanism-specific
treatment.
The most notable nonstructural syndrome is cytomegalovirus (CMV) polyradiculopathy in

immunocompromised individuals. Patients with this disorder present with a rapidly progressive
picture of usually asymmetric, bilateral radiating back and leg pain, weakness, incontinence,
and sensory loss. (See "AIDS-related cytomegalovirus neurologic disease".)
Herpes simplex may also produce a radicular syndrome of pain and paresthesias in a saddle
distribution.
Focal tumor such as schwannoma, or more diffuse tumor such as carcinomatous meningitis,
also can cause radicular problems. Inflammatory or infectious processes including Lyme
disease, syphilis, or sarcoidosis are rarely responsible.
Diabetes mellitus has been associated with inflammatory/ischemic radiculopathies in the

lumbosacral region. Patients generally present with what appears to be an acute structural
nerve root lesion with pain and some associated sensory loss and weakness. No lesion is
identifiable on imaging studies. Pain tends to be out of proportion to other objective signs.
Lumbar puncture may demonstrate an elevated protein and a mild lymphocytosis. Resolution of
this problem within weeks is typical. Nevertheless, evaluating for diabetes in patients with
radiculopathy of unknown etiology is reasonable. (See "Epidemiology and classification of
diabetic neuropathy".)

Identifying and treating the underlying disease is most important with any of the unusual forms
of inflammatory radiculopathy.
MISCELLANEOUS
Polyneuropathy — Polyneuropathies, both axonal and demyelinating, often preferentially

affect the lower extremities before beginning to seriously produce symptoms in the upper
extremities. Distal sensory loss, weakness, gait instability, and pain/burning in the feet
bilaterally are common symptoms. (See "Overview of polyneuropathy".)
Mononeuropathy multiplex — Ischemic lesions affecting multiple nerves may produce a

complex clinical picture. More widespread nerve involvement is present in most patients,
including in the legs. Nevertheless, in a sizable proportion of people this disorder may present
with a significant "axonal polyneuropathy" type picture in the legs [35]. (See "Clinical
manifestations and diagnosis of vasculitic neuropathies".)
Treatment of the underlying disease remains the rule. Recovery can be excellent despite initial
severe nerve damage.
Inflammatory demyelinating conditions — Certain disorders occasionally present initially

affecting one extremity. Chronic inflammatory demyelinating polyradiculoneuropathy may do
likewise. However, careful examination will reveal other abnormalities such as global hypo- or
areflexia or subtle weakness. (See "Chronic inflammatory demyelinating polyneuropathy:
Etiology, clinical features, and diagnosis".)
Zoster radiculoganglionitis — Patients with herpes zoster may develop, in addition to a painful
rash, weakness and sensory loss in a nerve distribution close to that of the rash. Inflammation
involves the nerve roots and dorsal root ganglion, potentially producing prominent neurogenic
injury. Electromyography (EMG) and nerve conduction studies (NCS) may reveal significant
sensory and motor abnormalities.
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more

sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Radiculopathy of the neck and back (including
sciatica) (The Basics)")
SUMMARY
● Anatomy and etiologies – Nerve roots emerge from the spinal column from the L2 to S4
levels through the neural foramina and join to form a complex entity known as the
lumbosacral plexus ( figure 1). The major mechanisms of lower extremity peripheral
nerve injury are compression, transection, ischemia, radiation exposure, inflammation,
and neuronal degeneration. (See 'Pathogenesis' above.)
● Clinical features and diagnosis – The clinical features of specific lower extremity nerve
syndromes are summarized in the tables ( table 1 and table 2). Electromyography
(EMG) with nerve conduction studies (NCS), neuroimaging, and laboratory testing can be
useful for identifying and classifying peripheral nerve disorders affecting the lower
extremity. (See 'Clinical presentation' above and 'Diagnostic testing' above.)
● Specific syndromes
• Fibular (peroneal) neuropathy – The typical clinical presentation of common fibular

(peroneal)/fibular neuropathy at the fibular neck is acute foot drop. (See 'Fibular
(peroneal) nerve' above.)
• Tarsal tunnel syndrome – Tarsal tunnel syndrome refers to tibial nerve compression in
the region of the ankles as the nerve passes under the transverse tarsal ligament
( figure 3). Patients typically present with aching, burning, numbness, and tingling
involving the sole of the foot, the distal foot, the toes, and occasionally the heel. (See
'Tibial nerve' above.)
• Sciatic neuropathy – Sciatic neuropathy occurs due to a variety of causes. In addition

to pain, patients with sciatic nerve injury in the sciatic notch/gluteal region complain of
weakness affecting most of the lower leg musculature. (See 'Sciatic nerve' above.)
• Femoral neuropathy – Femoral neuropathy also occurs due to a number of causes and
typically results in weakness involving the quadriceps with sparing of adduction. (See
'Femoral nerve' above.)
• Lateral femoral cutaneous neuropathy – Lateral femoral cutaneous nerve

entrapment as it traverses below the inguinal ligament produces the syndrome of
meralgia paresthetica, characterized by paresthesia and pain that radiates down the
lateral aspect of the thigh toward the knee. (See 'Lateral femoral cutaneous nerve'
above.)
• Obturator neuropathies – Mononeuropathies of the obturator nerve are uncommon.

They present with pain, weakness in leg adduction, and sensory loss over a small area
in the medial thigh. (See 'Obturator nerve' above.)
• Lumbosacral plexopathies – Lumbosacral plexopathies usually present with diffuse

weakness of the affected lower extremity, although a patchy distribution of weakness
may occur. The causes are numerous and diverse ( table 3). (See 'Lumbosacral
radiculopathy' above.)
• Diabetic amyotrophy – Diabetic amyotrophy and idiopathic lumbosacral

radiculoplexus neuropathy often present with asymmetric, focal onset of pain followed
by weakness involving the leg, with associated autonomic failure and weight loss.
Progression occurs over months and is followed by partial recovery in most patients.
(See 'Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy'
above.)
• Lumbosacral radiculopathy – Lumbosacral radiculopathy is a condition in which a

disease process affects the function of one or more lumbosacral nerve roots. The most
common etiology is nerve root compression caused by a disc herniation or spinal
stenosis. The symptoms and signs vary according to level ( table 1). (See
'Lumbosacral radiculopathy' above.)
• Other syndromes – Additional lower extremity peripheral nerve syndromes include

polyneuropathy, mononeuropathy multiplex, inflammatory demyelinating
neuropathies, and zoster radiculoganglionitis. (See 'Miscellaneous' above.)
Use of UpToDate is subject to the Terms of Use.
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Topic 5278 Version 31.0

GRAPHICS
Anatomy of the lumbosacral plexus
Graphic 75983 Version 1.0

Bony relationships of the nerve supply to the leg
Reproduced with permission by Patten, J. Neurological Differential Diagnosis, 2nd ed, Springer, London 1996.

Symptoms and signs of lumbosacral radiculopathies
Nerve Symptoms Signs
L5 Back pain radiating down the Decreased foot dorsiflexion, toe extension, foot inversion
lateral leg to foot and eversion; mild weakness of leg abduction in severe
cases
S1 Pain radiating down the posterior Decreased leg extension, foot inversion, plantar flexion, and
leg to foot; leg pain greater than toe flexion; decreased sensation in the posterior leg and
back pain lateral foot; loss of ankle jerk
L2-4 Acute back pain radiating around Decreased hip flexion, knee extension, leg abduction;
the anterior leg into the knee and decreased sensation in the anterior thigh down the medial
possibly foot aspect of the shin; diminished knee jerk in severe cases
S2-4 Sacral or buttock pain radiating Minimal weakness; bowel and bladder dysfunction
down the posterior leg or into the
perineum

Lower extremity peripheral nerve syndromes
Nerve Site of injury Cause Symptoms Signs
Common Fibular neck, Prolonged lying, leg Foot drop, Weakness on foot
peroneal just below the crossing, squatting, paresthesias and/or dorsiflexion and
knee leg cast sensory loss over eversion; sensory loss on
dorsum of foot and dorsum of foot; reflexes
lateral shin normal
Deep Ankle Tight fitting shoe rim Ankle pain, minimal Minimal
peroneal or strap weakness and
sensory loss over
web space between
digits 1 and 2
Posterior Tarsal tunnel of Fracture or dislocation Aching, burning, Positive Tinel's sign over
tibial ankle of talus, calcaneus, numbness, tingling nerve posterior to
medial malleolus, on sole of foot, medial malleolus;
rheumatoid arthritis, distal foot, toes, sensory loss on sole of
tumor and occasionally foot; atrophy of foot
heel muscles if severe
Sciatic Sciatic Trauma (hip Leg pain and Sensory loss in peroneal
notch/gluteal dislocation, fracture, weakness affecting tibial, and sural
region or replacement), most lower leg territories; may spare
prolonged bed rest, muscles medial calf and arch of
deep-seated pelvic foot; normal knee jerk;
mass, piriformis absent ankle jerk
syndrome
Mid-thigh Femur fracture, mass, Similar to above but Similar to above

ischemic nerve sparing hamstrings
infarction
Femoral Pelvis and Hip or pelvic fracture, Quadriceps Quadriceps weakness;

anterior thigh hip replacement, weakness and sensory loss over
lithotomy position, sensory loss anterior and medial
diabetes mellitus thigh extending down
medial shin to arch of
foot; reduced or
unobtainable knee jerk
Lateral Inguinal Obesity, tight fitting Paresthesias and Sensory loss on lateral
femoral ligament belts, idiopathic pain radiating down thigh
cutaneous (meralgia the lateral thigh to
paresthetica) knee

Tarsal tunnel anatomy
The tarsal tunnel syndrome is caused by entrapment of the posterior tibial nerve beneath the flexor
retinaculum on the medial side of the ankle. Entrapment may also include the two branches, the medial
and lateral plantar nerves. Note that the bifurcation of the tibial nerve, which is depicted occurring
proximal to the retinaculum in the diagram above, can occur more distally in the region of the
retinaculum.
Reproduced with permission from: Moshrefi S, Curtin C. Nerve repair and reconstruction—Tibial nerve. In: Operative Techniques in
Plastic Surgery, Chung KC (Ed), Wolters Kluwer, Philadelphia 2020. Copyright © 2020 Wolters Kluwer Health.

Causes of lumbosacral plexopathy
Diabetic amyotrophy (diabetic lumbosacral radiculoplexus neuropathy)
Idiopathic lumbosacral radiculoplexus neuropathy
Primary neoplastic invasion/compression
Metastatic cancer
Benign neoplasms
Radiation plexopathy
Ischemic plexopathy
Postoperative plexopathy
Retroperitoneal hematoma
Arterial (pseudo) aneurysm
Trauma
Obstetric (antepartum, intrapartum, postpartum)
Vasculitides
Connective tissue disorders
Sarcoidosis
Amyloidosis
Infection (eg, human immunodeficiency virus [HIV], Epstein-Barr virus, cytomegalovirus, varicella-zoster
virus, Lyme disease, syphilis)
Abscess (eg, tuberculosis, salmonella)
Heroin injection

Lumbosacral dermatomes
Schematic representation of the lumbosacral dermatomes. Patients with sciatica may have pain,
paresthesias, and diminished sensation in the dermatome of the nerve root that is involved.

Contributor Disclosures
Seward B Rutkove, MD Equity Ownership/Stock Options: Haystack Diagnostics, Inc [Electrical impedance
myography]; Myolex, Inc [Electrical impedance myography]. Patent Holder: Haystack Diagnostics, Inc
[Electrical impedance myography]; Myolex, Inc [Electrical impedance myography]. Grant/Research/Clinical
Trial Support: Haystack Diagnostics, Inc [Electrical impedance myography]; Myolex, Inc [Electrical
impedance myography]. Consultant/Advisory Boards: Haystack Diagnostics, Inc [Electrical impedance
myography]; Myolex, Inc [Electrical impedance myography]. All of the relevant financial relationships listed
have been mitigated. Jeremy M Shefner, MD, PhD Grant/Research/Clinical Trial Support: AB Sciences
[ALS]; Amylyx [ALS]; Biogen [ALS]; Cytokinetics Incorporated [ALS]; Ionis [ALS]; Mitsubishi Tanabe Pharma
America [ALS]; PTC [ALS]; QurAlis [ALS]; Sanofi [ALS]; Wave Life Sciences [ALS]. Consultant/Advisory Boards:
AcuraStem [ALS]; Amylyx [ALS]; Annexon [ALS]; Apellis [ALS]; Clene [ALS]; Cytokinetics [ALS]; Denali [ALS];
Eikonizo [ALS]; GSK [ALS]; Mitsubishi Tanabe Pharma America [ALS]; Neurosense [ALS]; Novartis [ALS];
Revalesio [ALS]; RRD [ALS]; Swanbio [ALS]; Vertex [DMD]. All of the relevant financial relationships listed
have been mitigated. Richard P Goddeau, Jr, DO, FAHA No relevant financial relationship(s) with ineligible
companies to disclose.
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Overview of Lower Extremity Peripheral Nerve Syndromes - UpToDate

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6/6/24, 13:47 Overview of lower extremity peripheral nerve syndromes - UpToDate

Official reprint from UpToDate®

Literature review current through: May 2024.

Compression — Compression (including neurapraxia and axonotmesis) is the most common

Radiation-induced injury — Radiation exposure, generally in the context of radiotherapy for

● An idiopathic inflammatory response is responsible for the syndrome of lumbosacral

● An inflammatory response associated with diabetes mellitus occasionally occurs, likely

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Degeneration — Distal degeneration of neurons is the hallmark of most axonal

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Electrodiagnostic studies — Electromyography (EMG) and nerve conduction studies (NCS)

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● Fasting glucose and glycohemoglobin in patients with possible diabetic amyotrophy,

● Lyme titers in patients with polyradiculopathy, especially in endemic areas

Lumbar puncture — Lumbar puncture is warranted in patients with unusual presentations of

FIBULAR (PERONEAL) NERVE

● Clinical features – The typical clinical presentation of common fibular (peroneal)

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● Treatment – In contrast to upper extremity neuropathies, treating compression

● Prognosis – Prognosis depends upon the degree of dysfunction. In one study of 13

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Sciatic neuropathy occurs due to a variety of causes.

● Other uncommon causes of sciatic neuropathy include childbirth, vascular malformations,

The piriformis syndrome is a controversial condition that may be an occasional contributor to

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Patients with diabetes mellitus occasionally develop spontaneous femoral neuropathies.

Needle electromyography (EMG) may be helpful in demonstrating isolated involvement of

● Management – The management of femoral nerve injury is mainly supportive and

LATERAL FEMORAL CUTANEOUS NERVE

● Management – Meralgia paresthetica is a self-limited, benign disease in most patients.

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● Diabetic amyotrophy and idiopathic lumbosacral radiculoplexus neuropathy (see "Diabetic

● Neoplastic invasion (see "Lumbosacral plexus syndromes", section on 'Neoplastic invasion')

● Radiation therapy (see "Lumbosacral plexus syndromes", section on 'Radiation

● Trauma (see "Lumbosacral plexus syndromes", section on 'Trauma')

● Pregnancy (see "Lumbosacral plexus syndromes", section on 'Peripartum plexopathy')

● Surgery (see "Lumbosacral plexus syndromes", section on 'Postoperative plexopathy')

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● Vascular conditions, particularly retroperitoneal hematoma (see "Lumbosacral plexus

● Parainfectious, inflammatory, and infiltrative disorders (see "Lumbosacral plexus

DIABETIC AMYOTROPHY AND IDIOPATHIC LUMBOSACRAL RADICULOPLEXUS

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Idiopathic lumbosacral radiculoplexus neuropathy is similar to diabetic amyotrophy with

affected, involvement of multiple myotomes is usually present in older people. Regardless

• L2-L4 radiculopathy – Localizing a midlumbar radiculopathy to a specific nerve root

• L5 radiculopathy – L5 radiculopathy is by far the most common radiculopathy

• S1 radiculopathy – In S1 radiculopathy, pain radiates down the posterior aspect of the

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treatment of acute lumbosacral radiculopathy is discussed in detail separately. (See "Acute

Nonstructural disease — Nonstructural causes are occasionally responsible for symptoms of

The most notable nonstructural syndrome is cytomegalovirus (CMV) polyradiculopathy in

Diabetes mellitus has been associated with inflammatory/ischemic radiculopathies in the

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Polyneuropathy — Polyneuropathies, both axonal and demyelinating, often preferentially

Mononeuropathy multiplex — Ischemic lesions affecting multiple nerves may produce a

Inflammatory demyelinating conditions — Certain disorders occasionally present initially

INFORMATION FOR PATIENTS

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• Fibular (peroneal) neuropathy – The typical clinical presentation of common fibular